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G/kg Alcohol (kg + alcohol)
Selected AbstractsInteractions between alcohol and caffeine in relation to psychomotor speed and accuracyHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 3 2002Michelle Mackay Abstract Unlike other CNS depressants, alcohol intoxication can be associated with increased error rates, coupled with unaffected (or speeded) response rates during psychomotor and cognitive processing. The present study examined whether concurrent consumption of caffeine may differentially affect these aspects of alcohol and performance. A randomised, double-blind, placebo-controlled design was utilised in which 64 healthy young volunteers received either 0.66,g/kg alcohol, caffeine (110,120,mg), both or neither. Performance was assessed using a four choice reaction time task (FCRT) with elements of repetitive (predictable) and random stimuli sequences and the digit symbol substitution task (DSST). Individuals on alcohol made significantly more errors during both fixed and random FCRT sequences, and there was evidence of weak antagonism of these effects by caffeine on the latter measure. On the DSST test of psychomotor speed, alcohol was associated with a significant slowing, the caffeine group were significantly faster and there was clear antagonism of the effects of alcohol by caffeine. These findings confirm that alcohol consumption is associated a greater number of errors and provide some evidence for task-specific antagonism of alcohol's cognitive effects by caffeine. Copyright © 2002 John Wiley & Sons, Ltd. [source] Alcohol Inhibits Spontaneous Activity of Basolateral Amygdala Projection Neurons in the Rat: Involvement of the Endocannabinoid SystemALCOHOLISM, Issue 3 2008Simona Perra Background:, A large body of evidence indicates that the limbic system is involved in the neural processing underlying drug addiction. Among limbic regions, the basolateral nucleus of amygdala (BLA) is implicated in some aspects of the neurobiological mechanisms of drugs of abuse, including alcohol and cannabinoids. It is recently emerging that the endocannabinoid system is involved in many pharmacological and behavioral effects of alcohol. The BLA possesses a very high density of CB1 cannabinoid receptors, and endocannabinoids modulate forms of synaptic plasticity in this region. The aims of our study were first to investigate in vivo the sensitivity of BLA pyramidal neurons to alcohol and second to determine the role of the endocannabinoid system in the acute effects of alcohol. Methods:, We utilized extracellular single cell recordings in urethane anesthetized rats from BLA principal neurons, antidromically identified from their projection site in the nucleus accumbens. Results:, Alcohol (0.25 to 2.0 g/kg i.v.) induced a marked decrease in the spontaneous firing rate of BLA projecting neurons (51.1 ± 16% of baseline at 0.5 g/kg alcohol, p < 0.0001). The involvement of the endogenous cannabinoid system was investigated by administering the CB1 receptor antagonist SR141716A (rimonabant, SR) (1.0 mg/kg i.v.) before alcohol. SR per se did not significantly affect firing rate of BLA neurons, but it prevented the inhibition produced by alcohol (98 ± 18% of baseline firing at 0.5 g/kg alcohol, p < 0.01). Then, we studied the actions of alcohol following a chronic treatment with the CB1 agonist WIN55212-2 (WIN). Animals were administered WIN for 6.5 days (2.0 mg/kg, i.p. twice daily) and alcohol dose,response curves were carried out on firing rate of BLA neurons 24 hours following the last injection of the cannabinoid agonist. In WIN-treated animals the inhibitory effect of alcohol was significantly reduced as compared with controls (95 ± 16% of baseline firing at 0.5 g/kg, p < 0.05). Conclusions:, Our results provide evidence of the involvement of the endocannabinoid system in the effects of alcohol on BLA projection neurons. They also further point to the endocannabinoid system as a possible molecular target in the treatment of alcoholism. [source] Neuroadaptations of Cdk5 in Cholinergic Interneurons of the Nucleus Accumbens and Prefrontal Cortex of Inbred Alcohol-preferring Rats Following Voluntary Alcohol DrinkingALCOHOLISM, Issue 8 2006Marguerite Charlotte Camp Background: Neurobiological studies have identified brain areas and related molecular mechanisms involved in alcohol abuse and dependence. Specific cell types in these brain areas and their role in alcohol-related behaviors, however, have not yet been identified. This study examined the involvement of cholinergic cells in inbred alcohol-preferring rats following 1 month of alcohol drinking. Cyclin-dependent kinase 5 (Cdk5) immunoreactivity (IR), a marker of neuronal plasticity, was examined in cholinergic neurons of the nucleus accumbens (NuAcc) and prefrontal cortex (PFC) and other brain areas implicated in alcohol drinking, using dual immunocytochemical (ICC) procedures. Single Cdk5 IR was also examined in several brain areas implicated in alcohol drinking. Methods: The experimental group self-administered alcohol using a 2-bottle-choice test paradigm with unlimited access to 10% (v/v) alcohol and water for 23 h/d for 1 month. An average of 6 g/kg alcohol was consumed daily. Control animals received identical treatment, except that both bottles contained water. Rats were perfused and brain sections were processed for ICC procedures. Results: Alcohol drinking resulted in a 51% increase in Cdk5 IR cholinergic interneurons in the shell NuAcc, while in the PFC there was a 51% decrease in the percent of Cdk5 IR cholinergic interneurons in the infralimbic region and a 46% decrease in Cdk5 IR cholinergic interneurons in the prelimbic region. Additionally, single Cdk5 IR revealed a 42% increase in the central nucleus of the amygdala (CNA). Conclusions: This study identified Cdk5 neuroadaptation in cholinergic interneurons of the NuAcc and PFC and in other neurons of the CNA following 1 month of alcohol drinking. These findings contribute to our understanding of the cellular and molecular basis of alcohol drinking and toward the development of improved region and cell-specific pharmacotherapeutic and behavioral treatment programs for alcohol abuse and alcoholism. [source] Fast, but Error-Prone, Responses During Acute Alcohol Intoxication: Effects of Stimulus-Response Mapping ComplexityALCOHOLISM, Issue 4 2004Tom A. Schweizer Abstract: Background: Although moderate doses of alcohol can impair performance on tasks that require information processing, little is known about the locus of the alcohol effects within the processing stream. This study used a psychological refractory period paradigm to investigate the effect of alcohol on the central, cognitive stage of information processing when task complexity is manipulated by altering stimulus-response compatibility. Methods: Thirty-four healthy male social drinkers were assigned to one of two groups (n= 17) that performed two tasks. Each trial consisted of a task 1 stimulus (tone) followed by a task 2 stimulus (letter) that was presented after one of four stimulus onset asynchronies (50, 200, 500, or 1100 msec). A baseline test of performance was obtained before the groups received a beverage containing either 0.0 g/kg (placebo) or 0.65 g/kg alcohol. Both groups were retested when blood alcohol concentration (BAC) was increasing and was decreasing. Results: The alcohol group made significantly more errors in task 1 compared with their drug-free baseline measure during the ascending phase of the BAC curve, and error rates increased to a greater extent for the more complex arbitrary stimulus-response mapping condition. Moreover, this increase in errors continued unabated during the descending phase of the BAC curve. Increasing BACs also slowed performance (longer reaction time), but unlike errors, reaction time returned to drug-free baseline levels when BAC was decreasing. Conclusions: The results provide evidence that an acute dose of alcohol can impair one aspect of the central, cognitive stages of information processing. The possibility that errors in information processing remain during decreasing BACs even after processing speed has returned to drug-free levels has important practical implications relating to the detrimental consequences of acute alcohol intoxication. [source] Fetal alcohol syndrome (FAS) in C57BL/6 mice detected through proteomics screening of the amniotic fluid,BIRTH DEFECTS RESEARCH, Issue 4 2008Susmita Datta Abstract BACKGROUND: Fetal Alcohol Syndrome (FAS), a severe consequence of the Fetal Alcohol Spectrum Disorders, is associated with craniofacial defects, mental retardation, and stunted growth. Previous studies in C57BL/6J and C57BL/6N mice provide evidence that alcohol-induced pathogenesis follows early changes in gene expression within specific molecular pathways in the embryonic headfold. Whereas the former (B6J) pregnancies carry a high-risk for dysmorphogenesis following maternal exposure to 2.9 g/kg alcohol (two injections spaced 4.0 h apart on gestation day 8), the latter (B6N) pregnancies carry a low-risk for malformations. The present study used this murine model to screen amniotic fluid for biomarkers that could potentially discriminate between FAS-positive and FAS-negative pregnancies. METHODS: B6J and B6N litters were treated with alcohol (exposed) or saline (control) on day 8 of gestation. Amniotic fluid aspirated on day 17 (n = 6 replicate litters per group) was subjected to trypsin digestion for analysis by matrix-assisted laser desorption,time of flight mass spectrometry with the aid of denoising algorithms, statistical testing, and classification methods. RESULTS: We identified several peaks in the proteomics screen that were reduced consistently and specifically in exposed B6J litters. Preliminary characterization by liquid chromatography tandem mass spectrometry and multidimensional protein identification mapped the reduced peaks to alpha fetoprotein (AFP). The predictive strength of AFP deficiency as a biomarker for FAS-positive litters was confirmed by area under the receiver operating characteristic curve. CONCLUSIONS: These findings in genetically susceptible mice support clinical observations in maternal serum that implicate a decrease in AFP levels following prenatal alcohol damage. Birth Defects Research (Part A), 2008. © 2008 Wiley-Liss, Inc. [source] | ||||||||||